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fitbyfred

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 #16 
Ruud_G, hi. Yes, absolute info would be terrific... the fun with MOXY NIRS seems to be in the relative trends--and yes, the supporting info.

I do have many supporting info for this case (tHb, SpO2, RF, vT, VE, SEMG & RPE) however I was aiming to post it slowly.

The reason for this:

1) I'm super keen to see what we can discuss/interpret at the simplest level of info 
2) Was trying to follow the spirit of this topic, which seemingly was starting off with HR/SmO2
A;omg with your earlier suggestions, which were great, we should try to determine best etiquette to keep a topic moving forward along it's initial idea/context/theme ???

What do others think ? 


juergfeldmann

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 #17 
Thanks  as usual  for the   great  discussion.  Here the funny  part :


Hi Juerg. Wrt diving into how to measure stroke volume, etc. maybe a good idea to stay at the metrics which the person (in this case NO) had.  

This is  so great  with NIRS. If  we stay  with the metrics  from MOXY  like SmO2  and  tHb  and perhaps we add HR  and wattage  we already  have a huge amount of information.
 Now  as  so often  if  we try  to show  we   are  relative confident  that we  can make  feedback's  on CO  and  VE  and more , that the interesting  proper  respond  comes, whether we  can proof  or  support this ideas.


 Again and again.  where are the same  positive  critical points  when  we  use what is  on the market now. How  do people support a  lactate threshold  with an  idea , based on 4 mmol  or on 1 mmol increase per  step  or a tangent  against a  " curve  or  a  %  of VO2  max.
 I see never  ever a critical  discussion on this  we simple take it load it   so take  75  %  of FTP  tested  3 weeks  ago  and still believe  and trust , that it  suppose to trigger the same  physiological feedback. The  beauty now is , you see it  and you know it  and you can correct.
 So  the  question really is , why we have   so much  problems  and discussion  to open  some minds  to at least  try  compare  and fairly ask the same  questions in what  you  or he  or she is doing  now  . Than  even make a  cost  and benefit  analyses  and think  again.
 Thanks  to  Fred , Ruud , Daniele and many more on here,  we  can slowly  but surely  show that there  is  some merits  in at least looking  at MOXY   just to  compare  and be sure  what we did in the past is    at least  as nice  or  could at least  partially benefit  from some feedback  by NIRS.    Summary :
 Dilemma  and  beauty
 Shall we  stay  simple  

Hi Juerg. Wrt diving into how to measure stroke volume, etc. maybe a good idea to stay at the metrics which the person (in this case NO) had.


or   do we go again complex  and get   points back  to make it simple ( Smile ).

CO (cardiac output) is still upheld. Might as well be that stroke volume went down. We don't know. same wrt respiratory changes (we don't know, only hypothesis). Maybe Juerg / someone else can chime in wrt the respiratory hypothesis regarding this.

But to come back to the "HR arena" from a delivery perspective here tHb comes in. I wish we could see absolutes.... (But we can't...;(


 This is  where we  go complex the last  few  years to avoid the discussion,  that we simply have a hypothesis  as we look  for  actual feedback.
 But than again  the question  from many,  can I simply  just use  MOXY  for all this information. Do I need a  big   knowledge in physiology  and so on. ?
 Answer  YES in many cases  and yes  we  can show  with complex  tools that  MOXY  can give you this feed backs.  So   it is a  interesting  situation  when introducing  a new kid on the block , we like to  be nice  and accept and welcome it, but than we still hesitate  and like first  to know  more before  we commit. Pretty  normal  isn't  it ? 
Solution:
  we will keep doing both , so new readers  can   move  slowly in  and  the top   guys  on here  can help  to critically   use  and  move forward  so we all  keep improving.
Ruud_G

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 #18 
Hi Fred. Fully Agree. Good thing to keep it simple at first!!
juergfeldmann

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 #19 
iI like to keep the discussion here going as we  agree  not to agree to easy on the   term of High intensity  as this is a fundamental  question at least for me  during practical applications  for any  person.   Simple example  which may make  sense  I hope.
 I have a  cyclists  crashed ( not  that unusual )  and he has a  huge road  rash  and   can simply  not bike for  at least  another few  days  but  for sure not the intensity he had planned  to  do  for his upcoming race. in 10  days.
 What  not to worry about  first.
a )intermuscular coordination  as he did  millions  of  motions  over and over.
b) intramuscular coordination. yes  that  could start to get somewhat lost  depending on the  athlete  and his  type  of intramuscular  workouts  his coach may  use. 
 So we will use   Compex  or  any other   specific  muscle fibre type    stimulation  for his main muscles. Maintain  intramuscular  contraction  and in some cases even up regulate the pattern.
c) Respiration  Yes  that could be some loss there  so  simple to  maintain   even VE  volume   of  250 plus liter    by  using  any  available   normocapnic  hyperpneu  equipment. During. The  use of this  is   the same frequency  as your coach  had planned  do  to certain on  bike workouts.
d) Cardiac load.
 Yes  for sure  close to maintained  but  harder  to  get frequency  but easier  to  stress SV  and  or  right or left  ventricle.
e)   high intensity

Now we are here, where we lost  or gained the NO  case.
 What is considered  high intensity.
 1. Is it   by just looking  at outside  load like wattage  and anything above FTP  may be considered  high intensity.
2. Is it  by just looking  cardiac  load  so highest  CO  is  High intensity ? and here  is it higher if   we have  a high HR  or  a high SV
3. Is it looking how respiration reacts  so highest or very high VE and here if we  have a high RF  or  a high TV
4. Is it high  when we have a high VO2  number  So you can see many questions.

  Or
  when using NIRS , should we look at  the energy  supply  and utilization situation.  I  do not have  an answer  so that's where we have some  needs  for  some clarifications.

Your  turn


 


DanieleM

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 #20 
Just a couple of observation regarding this 5/1/5.

  1. This has already been highlighted by Ruud: last two doubesteps have a quite different trend in terms of SmO2.The penultimate doublestep shows a slight decrease of SmO2.I would guess is an intensity she can keep for a while. The last doublesteps show instead a steep decrease, so there is no homeostasis at all. The fast decrease through the loads may means a continous shift to the right of the dissociation curve probably due to H+ accumulation, decreasing PH, increasing CO2.Again my guess is that this intensity could not be hold for a while and could be close to her VO2max.
  2. the SmO2 at the last steps are still quite high (higher than at the start).

One option is that she has a very good delivery system but low oxydative potential.
juergfeldmann

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 #21 
Daniele  as usual    perfect  thoughts  and absolutely  nothing   against this.
 The  interesting section  where I  am not sure is the   shift of the O2  disscurve to the right.
 This would be a  systemic  reaction in most cases  so an additional moxy on a non involved muscle would  give some feedback. The other place  I would look is a closer look at the rest  1 min reaction.
 Here  what happens.  Higher CO2  is a  very potent  vasodilatator. So  when we stop the one minute suddenly  we have  immediately no muscle contraction or at least much less contraction pressure  so  CO  is  still high  and therefore  we will have an increase  rapidly in tHb. As well we   will have  additional a vasodilatation  so  we will see  an overshoot in tHb  above  the levels   we reached  prior  to the  CO2  accumulation. So  we will look at his in the tHb  discussion.
 Additionally  we  may see an ongoing  drop in SmO2  despite  an overshoot in tHb   when we stop as  we may  be in a slightly  EIAH.   So we may see a delay in  SmO2  recovery  after the tHb  recovery  started.
 Now this is very clear in extreme situations. We  can have any situation in between. The  key here  for an indication of a   potential limitation  at the end in respiration is  the tHb overshoot  and the drop in  SmO2. So yes the  picture , when looking at  SmO2  can indicated this. So here a great idea is  to look to get feedback on respiratory  frequency  as an  easy  additional point could  be  using a SpO2  sensor   ( N. O  will geet one this week  as  a thak you for sharing the information with all of  us ) . So  this would be a simple tool .  More complex  is  VE  and RF  x  TV  feedback or we use very often  a  caponmeter so we have RF  and directly EtCO2 . This is risky  as  when we  reduce  TV  we often see a  drop in EtCO2  at the mouth level exactly because we increase in the body  so  CO 2 stays in  and is not moving through the mouth. That's  where VO2  an give some delays and  wrong  conclusions.
 VO2  max.  In a step test we never reach optimal VO2  max  at all but VO2  peak  in this case.
 In fact reverse  step tests  or   my old idea of lactate balance point protocol show  much higher Vo2  levels in the second section of the test  so higher than  at the VO2  step test information. There is as well a big study  done  from south Africa. On this subject  showing a  4 % +  increase  in VO2  in the second stage of the reversed  step test. Again throwing into  question the concept  of VO2  max testing and a VO2  max  plateau.  Remember one of the latest revies  on this show a nearly 50 %   situation, where VO2  max  never  was found or reached  even using many  strange criteria  todefend a  Max value  to   save those classical idea.
Ruud_G

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 #22 
Well. In terms of NIRS what would denote the HII "zone". I would say that in general it must be somewhere where there is a progressive loss of homeostasis. It should represent a boundary or ceiling after which you say: this is sustainable exercise and this not.

So. A progressive loss of SmO2? Quite vague. I know. And linking this to some 5-1-5s I have seen it wouldn't fit: for some you could, for some you can't. Maybe a different protocol nex to TIP if you can't determine it easily? Just thinking out loud.

End of the day I believe that the boundary could be (or should?) based as from where you would see a continuous growth of VO2 until you reach VO2max after a homeostasis. We we don't measure this normally with NIRS equipment only.

But I think we're moving into the direction "off topic"? Maybe "zoning" should be a complete seperate thread. And as said: just thinking out loud.

But as said before maybe tHb can throw in some more light. Although that does (or does not have to coincide with my thoughts [wink]
juergfeldmann

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 #23 
Ruud great  loud thinking   I love it as it  sounds  like in my brain  lot's of  things  going on  and it is  fun  to discuss this  option  and yes it would be great  finding a  kind of definition  for simplification. On the other side when using it practically, you will see  and feel it and you k now it is high intensity and  not sustainable.
 I really encourage  all MOXY owners,  to  do  a simple   biceps  contraction idea  and play with it  and see  whether your feeling of   end of  strength  is   relating  the  SmO2  trend.  and than come back here  and share.
fitbyfred

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 #24 
What is high intensity? 

In my gym the RPE posters have 10 at the top. The caption below reads, Impossible for You to Persist. 

Below this are 9 - 1 in descending order with various descriptors of limb muscle and/or breathing fatigue, etc etc. The caption below the 1 rating reads, You Can Continue indefinitely.

The 1 & the 10 ratings are the only two that I find continuously reliable.

I'd say a high intensity performance, whether repeated many times or for just a couple is going to be marked by a little (start), by a lot (middle) or by maximum compensation (end) to persist.

Here's a nice example of an outwardly seen compensation.  

sprint_1.jpg 

As for workout intensity guidance, the higher the load quality we use, I can see super-fast the direct local shift of tHb and SmO2 trend, which is great! This so far is one of the easiest markers of quality / HII that I have used over two and half decades. When we look to add other biometrics, such as HR, RF, SpO2 (better of the 3 I think), we can definitely add nice info, but for depending on individuality it can reduce clarity.

As per picture above, they look a little like an all-out effort. I wonder what the MOXY info would show ?      


fitbyfred

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 #25 
Ruud_G, hi. Here is the next layer of the cycling 5 1 5 where based on the HR and the SmO2 we asked the question, is the final 4 steps an FEI or HII load ? See here now with tHb performance line:

FEI or HII?.jpg 

Recall as well we discussed a couple of contrary HII inclusion/exclusion ideas: 

1) the cyclist was able to persist through all 5 min loads
2) the %SmO2 shows steep and (decently) deep drop to roughly 23-25% 

Thoughts ?

juergfeldmann

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 #26 
As  well it shows  a very fast  SmO2  recovery. Here a hint  what I ma often looking over.
 I  overlap the recovery  sections    form start to  end  and look , whether there is a  clear  change in the slope  of the recovery SmO2 increase.
 I  do the same in interval loads  with complete  or   low intensity  recovery  ideas  as long the intensity  ( yes I use  wattage  on a bike ) is stable .
I  do the same  when reassessing over  a few  weeks or month the  same athlete.
 What  is the reading . I got pushed on this idea  by this  smart   guys  here.  

Skeletal Muscle Metabolism in Endurance Athletes with Near-Infrared Spectroscopy

JARED TODD BRIZENDINE, TERENCE EDWARD RYAN, REBECCA DANTE LARSON, and KEVIN K. MCCULLY

Department of Kinesiology, University of Georgia, Athens, GA

ABSTRACT

BRIZENDINE, J. T., T. E. RYAN, R. D. LARSON, and K. K. MCCULLY

. Skeletal Muscle Metabolism in Endurance Athletes with

Near-Infrared Spectroscopy. Med. Sci. Sports Exerc., Vol. 45, No. 5, pp. 869–875, 2013. Purpose: To determine whether near-infrared spectroscopy (NIRS) measurements of muscle mitochondrial function could detect the expected differences between endurance-trained

athletes (n = 8) and inactive subjects (n = 8). Methods: Muscle oxygen consumption (mV˙ O2) of the vastus lateralis was measured with continuous-wave NIRS using transient arterial occlusions. The recovery rate of mV˙ O2 after electrical stimulation was fit to an exponential curve, with the time constant (Tc) used as an index of mitochondrial capacity. Whole-body peak oxygen uptake was determined by indirect calorimetry during a continuous ramp protocol on a cycle ergometer. Results: Whole-body peak oxygen uptake values for endurance-trained and inactive controls were 73.5 T 9.1 and 33.7 T 5.9 mLIkgj1Iminj1, respectively (P G 0.001). The recovery rates of mV˙ O2 after exercise for endurance training were 18.4 T 3.2 and 18.8 T 2.5 s, whereas those for inactive controls were 32.4 T 5.2 and

34.9 T 5.9 s for the shallow and deep channels, respectively (P G 0.001 for comparison between groups). Resting mV˙ O2 was 0.52%Isj1 T 0.22%Isj1 for endurance athletes and 0.77%Isj1 T 0.82%Isj1 for inactive controls (P = 0.42).  

Conclusions:
The recovery rates of mV˙ O2 after exercise in endurance athletes were almost two fold faster than inactive subjects measured with NIRS, consistent with previous
studies using muscle biopsies and magnetic resonance spectroscopy.
Our results support the use of NIRS measurements of the recovery of oxygen consumption to assess muscle oxidative capacity.
Key Words: NIRS, MITOCHONDRIAL CAPACITY, ELECTRICAL STIMULATION, OXIDATIVE METABOLISM, ENDURANCE TRAINING, MAXIMAL OXYGEN UPTAKE, COMPETITIVE CYCLISTS


I  compare  if  always possible pre  and post op  clients  so  people  who can not  use a muscle  for a  longer duration  and if possible get them in  before they  have this   forced rest. The  change in SmO2  but as well as in tHb reactions is   interesting to follow.

Here  an example .of a right leg  and a left leg  post ops.
 Before  ops the left  and right were very equal  and the   left leg  was the dominate  leg

pp nirs.jpg  And below  to show  how we use it in   different applications to assess recovery  but as well changes over time.
overlap super clsoe flah.jpg 

  

next up 
  
swim overlap   low.jpg


This  may help  for  many  somewhat more , when we look at the I min rest  sections. We look  at :
  tHb reaction   . ( occlusion , CO2  help , and so on )  we look at SmO2  and you can see on the slop  but as well  on  immediate increase delayed increase    back to  base line  or  overshoots.
 So you  can see we slowly but surely  start to  see more and more information's  from  NIRS feed backs. And  we  will get more and more  high top confirmation on the practical use  we  r try to introduce  with using NIRS.   Remember  before MOXY  NIRS  was just  really  available  and used in many labs  and studies  due to the pricing  .  Even than  a  great NIRS  was only 14'000  %  so  similar like a VO2  or  any other  testing options. Now  you can do it  with 2  MOXYs  for a  small portion of the  former  pricing.

 The next step is   just getting confident on how you can use it  either in combination in what you always did  or  new  as  a new  user   in your  test center or training center or  as a coach.

juergfeldmann

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Posts: 1,501
 #27 
Here a feedback  to Ruuds  interesting   and  absolutely accepted  question of tachycardia.
 As  so often I had  to go back to my  original    work in  Bern  and  found this  study  which was  somewhere in my brain. About the tachycardia    and again  I  do not  say  N.O  has this . I   just said  it is interesting  and need  some  confirmation over a  set off exercises  to see,   how often  if  very it shows  up  again. 
The  top guy to ask   for  more back ground info  would be  Jiri  Dostal  from Prag  and he may  perhaps read this  and give his  great information to this  possible options  we may se once in a  while  on so  called healthy young athletes.
 

Tachyarrhythmias in Young Athletes

ALDO COELHO, MD, FACC, EDWIN PALILEO, MD, FACC, WILLIAM ASHLEY, MD, STEVEN SWIRYN, MD, FACe. A. TOM PETROPOULOS, MD, FACe. WILLIAM j, WELCH, MD, FACC, ROBERT A, BAUERNFEIND, MD, FACC

ChicaKU, llIinuis

Nineteen young athletes with documented symptomatic tachyarrhythmia were systematically evaluated. There were 15 men and 4 women, aged 14 to 32 years (mean 22 ± 6). Documented tachyarrhythmias were parox• ysmal atrial fibrillation in five patients, paroxysmal supraventricular tachycardia in five, paroxysmal ven• tricular tachycardia in eight (sustained in five, nonsus• tained in three) and ventricular fibrillation in one pa• tient. Abnormal substrates were demonstrated in 15 (79% ) of the 19 athletes: 5 had an anomalous atrioventricular (A V) pathway and 10 had heart disease (mitral valve prolapse in 9 patients and dilated cardiomyopathy in 1 patient). In 13 (68%) of the 19 athletes, all spontaneous attacks of tachyarrhythmia had started during strenuous  exercise. Tachyarrhythmia that closely resembled clin• ical arrhythmia was induced by programmed cardiac stimulation in 13 athletes (68%) and was reproducibly provoked by treadmill exercise in 8 athletes (42 % ). In four of seven athletes with ventricular tachycardia, tachycardia closely resembling clinical arrhythmia was provoked by infusion of isoproterenol. In summary: 1) young athletes can have any of several tachyarrhythmias; 2) abnormal substrates can be dem onstrated in many athletes with symptomatic tachyara rhythmia; and 3) tachyarrhythmias in young athletes frequently occur during exercise. (J Am Coil Cardiol 1986;7:237-43)

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